Journal of Clinical Microbiology, February 2009, p. 287-293, Vol. 47, No. 2
0095-1137/09/$08.00+0 doi:10.1128/JCM.01531-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Departments of Microbiology,1 Obstetrics and Gynaecology,2 Anatomical and Cellular Pathology,3 Community and Family Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong Special Administrative Region, People's Republic of China4
Received 8 August 2008/ Returned for modification 10 October 2008/ Accepted 15 November 2008
The clinical value of viral load and integration testing for human papillomavirus (HPV) remains unclear. Data on HPV type 18 (HPV18) is limited. We examined the HPV18 viral load and integration status of 78 women with normal cervix or neoplasia. While the crude viral load appeared to increase with lesion severity, the association was not significant after normalization with sample cellularity. Unlike reports for HPV16, the amino-terminal 1 region of HPV18 E2 was most frequently (71.0%) disrupted, representing the best marker for integration. A substantial proportion (57.1%) of invasive cancers harbored only the episomal genome, thus jeopardizing the clinical value of integration testing. A large proportion (41.7%) of normal/low-grade lesions showed viral integration, suggesting that integration of HPV18 starts early and is unlikely to be a sole determinant for progression. Interpretation of viral load should take into account the form of HPV infection as single infections had significantly higher viral loads than coinfections (P = 0.046). More data generated from routinely collected samples are warranted to verify the clinical value of viral load and integration testing. Viral load quantitation for HPV18 is premature for clinical use at this stage.
Published ahead of print on 26 November 2008.
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